Martens and colleagues (submitted, 2020) have demonstrated that L. casei AMBR2 could increase epithelial barrier function in primary cell layers derived from CRSwNP (CRS with nasal polyps) patients via upregulation of the same tight junction proteins, presumably through a TLR-2 mediated mechanism. The gene discussed is TLR2; the disease is chronic rhinosinusitis with nasal polyps.